PRESSURE-OVERLOAD INDUCED IN NEWBORN RATS - EFFECTS ON LEFT-VENTRICULAR GROWTH, MORPHOLOGY, AND FUNCTION

Citation
F. Kolar et al., PRESSURE-OVERLOAD INDUCED IN NEWBORN RATS - EFFECTS ON LEFT-VENTRICULAR GROWTH, MORPHOLOGY, AND FUNCTION, Pediatric research, 43(4), 1998, pp. 521-526
Citations number
30
Categorie Soggetti
Pediatrics
Journal title
ISSN journal
00313998
Volume
43
Issue
4
Year of publication
1998
Pages
521 - 526
Database
ISI
SICI code
0031-3998(1998)43:4<521:PIINR->2.0.ZU;2-K
Abstract
Gradual pressure overload was induced by abdominal aortic constriction in male rats on postnatal d 6 (AC6) or 2 (AC2). At the age of 8 wk, t he systemic blood pressure was measured, and the contractile performan ce of the left ventricle (LV) was assessed after acute ligation of the ascending aorta in open chest anesthetized animals. The LV free wall was used for the determination of collagen concentration and morphomet ric analysis of cardiac myocytes and capillaries. Aortic constriction resulted in LV hypertrophy, which was more pronounced in AC2 (by 71%) as compared with AC6 (by 34%) groups and correlated closely with the d egree of pressure overload (r = 0.88 and 0.80, respectively). The righ t ventricular weight was increased by 13% in the AC2 group only. Contr actile performance of the LV of aortic constricted rats was significan tly higher before as well as after the acute load, but the average fun ctional reserve was unchanged in both experimental groups. Although th e maximum value of the rate of pressure development increased linearly with the degree of ventricular hypertrophy in the AC6 group (r = 0.82 ), a negative correlation was observed in the AC2 animals (r = -0.61). The density of myocytes was decreased, and the calculated average myo cyte cross-sectional area was increased in aortic constricted rats, bu t the coronary capillary density and myocardial concentration of colla gen remained constant. Thus, in spite of the larger cardiac growth res ponse in the younger age group, the capillary proliferation and collag en formation were proportional to the ventricular hypertrophy. Therefo re. the degrees of overload and hypertrophy do not seem to be limiting factors. Pressure overload induced in newborn rats can be a useful mo del for the study of mechanisms that control either the growth and dif ferentiation of myocardium soon after birth, as well as the transition from compensated to decompensated hypertrophy at later stages.